Evidence map›Paper›PMID 25040398›Full record

ReviewClinical and experimental pharmacology & physiology2014

Cardiac alternans and intracellular calcium cycling.

Joshua N Edwards, Lothar A Blatter

Abstract readReview
In one paragraph

Review in Clinical and experimental pharmacology & physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed.

  1. A Beginner's Guide to Cardiac Optical Mapping.Cardiovascular engineering and technology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Atrial arrhythmogenesis and electrophysiological remodeling in hypokalaemic metabolic syndrome: the role of apamin-sensitive SK channels.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Protective Mechanisms of SGLTi in Ischemic Heart Disease.Journal of cardiovascular translational research · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Joshua N EdwardsDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL, USA.
Lothar A Blatter

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
E/C COUPLING AND CALCIUM REGULATION IN ATRIAL MYOCYTESR01HL062231 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI BLATTER, LOTHAR A · 1999 to 2012
$4.4M
MItochondrial Dysfunction in Cardiac Hypertrophy and FailureR01HL101235 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BERS, DONALD M, BLATTER, LOTHAR A · 2010 to 2013
$2.8M
NHLBI NIH HHS HL101235NHLBI NIH HHS HL62231NHLBI NIH HHS HL80101NHLBI NIH HHS P01 HL080101NHLBI NIH HHS R01 HL062231NHLBI NIH HHS R01 HL101235
6 · The paper itself

Abstract

Cardiac alternans refers to a condition in which there is a periodic beat-to-beat oscillation in electrical activity and the strength of cardiac muscle contraction at a constant heart rate. Clinically, cardiac alternans occurs in settings that are typical for cardiac arrhythmias and has been causally linked to these conditions. At the cellular level, alternans is defined as beat-to-beat alternations in contraction amplitude (mechanical alternans), action potential duration (APD; electrical or APD alternans) and Ca(2+) transient amplitude (Ca(2+) alternans). The cause of alternans is multifactorial; however, alternans always originate from disturbances of the bidirectional coupling between membrane voltage (Vm ) and intracellular calcium ([Ca(2+) ]i ). Bidirectional coupling refers to the fact that, in cardiac cells, Vm depolarization and the generation of action potentials cause the elevation of [Ca(2+) ]i that is required for contraction (a process referred to as excitation-contraction coupling); conversely, changes of [Ca(2+) ]i control Vm because important membrane currents are Ca(2+) dependent. Evidence is mounting that alternans is ultimately caused by disturbances of cellular Ca(2+) signalling. Herein we review how two key factors of cardiac cellular Ca(2+) cycling, namely the release of Ca(2+) from internal stores and the capability of clearing the cytosol from Ca(2+) after each beat, determine the conditions under which alternans occurs. The contributions from key Ca(2+) -handling proteins (i.e. surface membrane channels, ion pumps and transporters and internal Ca(2+) release channels) are discussed.

Indexed as

Blood PressureCalciumHeartHeart Conduction SystemHumansMyocardiumMyocytes, CardiacCalciumaction potentialarrhythmiaCa2+ regulationcardiac alternansexcitation-contraction couplingrestitution

Identifiers

PMID25040398
PMCPMC4122248

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.